44 Chapter 2 lack of proliferative capacity in terminally differentiated cardiomyocytes is somewhat in line with developmental studies illustrating that Hippo signaling controls cell-cycle arrest in adult cardiomyocytes (Xin et al., 2011; Wang et al., 2014). Genetic modification of the Hippo/ YAP signaling pathway results in dedifferentiation of adult myocardium with a subsequent regenerative response to ischemic injury (Leach et al., 2017; Monroe et al., 2019). Combined with novel DNA, RNA or nanoparticle local delivery technologies, signaling pathways hold promise as druggable targets in cardiovascular medicine (Braga et al., 2021). Future hiPSC-CM studies should focus on further simplification of the exact cues required for cardiomyocyte production, and should incorporate other myocyte subtypes required for regional repair of the heart, as well as more specific cardiac tissue generation. Disclosures J.W.B. and S.M.W. hold a patent on the expansion of hiPSC-derived cardiomyocytes. Acknowledgments R.G.C.M. is supported by a fellowship from the Stichting PLN. F.W.v.d.D. acknowledges support from the Dutch Cardiovascular Alliance. Q.Y. is supported by PhD fellowship from China Scholarship Council (201706170068). J.v.d.V. is supported by grants from Nederlandse Organisatie voor Wetenschappelijk Onderzoek–ZonMw (91818602 VICI), ZonMw and Hartstichting for the translational research program, project 95105003; the Dutch Cardiovascular Alliance grant Double Dose 2021; the Fondation Leducq grant number 20CVD01; and Proper Therapy project funded by the Nederlandse Organisatie voor Wetenschappelijk Onderzoek, domain Applied and Engineering Sciences (NWO-AES), the Association of Collaborating Health Foundations (Health~Holland), and ZonMw within the human models 2.0 call. S.M.W. is supported by the National Institutes of Health/National Institute of General Medical Sciences (1RM1GM131981-03); American Heart Association Established Investigator Award; Additional Ventures Foundation; National Science Foundation RECODE Project; and the Joan and Sanford I. Weill Department of Medicine Endowed Scholarship Fund. J.P.G.S. is supported by H2020-EVICARE (725229) of the European Research Council and ZonMw PSIDER grant (10250022110004). J.W.B. is supported by a Dekker Senior Clinical Scientist personal grant from the Hartstichting (03-003-2021-T025); Netherlands Heart Institute Fellowship; and CVON-Dosis young talent grant from the Hartstichting (CVON-Dosis 2014–40). Deposited in PMC for release after 12 months.
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